Memo To PZ Myers: Damage is Random. Repair is Not.

Atheist and Darwinian evangelist PZ Myers responded to my annotated transcript of our radio & podcast debate.

If one only reads PZ’s blog, skips past my transcript and doesn’t read Barbara McClintock’s work, one might form the impression that PZ gave that poor naïve engineer Perry Marshall a sound thrashing.

In actuality,

while doing a credible job of explaining part of McClintock’s work (for which I happily give him props) he further misrepresented what I wrote…

…And the role of McClintock’s landmark discovery, transposition; and her views of the cell; and biological cause and effect.

PZ would have you think I slunk into his office to bemoan my bad grade, as though he’s the professor here. Au Contraire, PZ. I’m taking you and the other old-school Darwinists to the woodshed for promulgating a version of evolution that’s 70 years obsolete.

Nobel Prize winner and eminent scientist Barbara McClintock is the professor of this class. Not you, PZ.

Dear reader, I simply ask you to compare what PZ says she said to what she actually said. Let’s begin with PZ’s misrepresentation of me:

[Perry] claims that she was denying the existence of chance events in genetics — that everything was about patterned, engineered information, which is the damnedest interpretation of McClintock.

Nobody is denying the existence of chance events. Especially external threats. All kinds of disasters confront organisms: Heat, cold, genome damage, starvation, chemicals. Internal and external accidents, stimuli from foreign organisms: insects, bacteria, fungi, etc.

Most or all these events may be completely random with respect to what the cell was already up to that day.

What’s not random is the cell’s response to the threat. Damage is random. Repair is not.

That is the point of my book Evolution 2.0. McClintock’s discoveries play a key role in distinguishing real-world evolution from the 1.0 version that Darwinists have been teaching for decades.

What Barbara McClintock was interested in – what her Nobel Prize paper was all about – was a burning question:

“What does the genome do in response to shocks for which it is unprepared?”

Please understand that cells fixing broken DNA strands was a secondary topic in her Nobel Prize paper. The primary focus was: How is the genome restructured by the cell, for the purpose of maintaining, surviving and adapting to the threat?

She is speaking from background knowledge that cells restructure their DNA in specific, programmed, predictable ways to common threats like heat and DNA damage.

Notice this is also the wider context for transposition, the discovery for which she won the Nobel Prize – that cells re-arrange DNA in direct response to threats, stress, and shock. Transpositions are by their very description non-random patterns of DNA editing.

McClintock was a hacker. What she was most interested in was: “What happens when I throw the system a curve ball? What if I do something that the system is not pre-programmed to respond to?”

PZ’s blog implies that chromosomes break in random ways; cells repair them by haphazardly patching them back together, they break again in even more random ways, and you get variation. Variation gives natural selection stuff to work with, and presto, you get evolution.

The problem with that is, cells don’t just randomly stick stuff back together. All you have to do is examine the diagrams of transposon behavior to see that there are specific regions (donor DNA, target DNA, genes, transposons, telomeres) which have specific jobs, subcomponents, and start and end points.

Chromosomes have very specific structures, and cells re-assemble damaged genomes according to the rules of the structures. It’s the re-assembly according to rules that creates useful variation.

PZ Says…

Barbara McClintock Says…

McClintock talks about stress-induced reorganization of the genome, and [Perry] leaps to the conclusion that she’s describing a teleological phenomenon in which the genome reshapes itself directly to address the circumstances, when every process she actually describes is about increasing variation.

The ability of a cell to sense these broken ends, to direct them toward each other, and then to unite them so that the union of the two DNA strands is correctly oriented, is a particularly revealing example of the sensitivity of cells to all that is going on within them. They make wise decisions and act upon them.

For instance, he’s obsessed with transposition. He thinks this is engineering.

Time does not allow even a modest listing of known responses of genomes to stress that could or should be included in a discussion aimed at the significance of responses of genomes to challenge.

We can take advantage of that by making a gene of interest the ‘chunk’ and getting it to insert somewhere. Somewhere random. That’s the whole point. These are called jumping genes for a reason.

In addition to modifying gene action, these elements can restructure the genome at various levels, from small changes involving a few nucleotides, to gross modifications involving large segments of chromosomes, such as duplications, deficiencies, inversions, and other more complex reorganizations.

McClintock’s triumph was being able to explain random variation within an organism that by convention ought to be genetically uniform by mechanistic processes like transposition and bridge-breakage-fusion.

The responses of genomes to unanticipated challenges are not so precisely programmed. Nevertheless, these are sensed, and the genome responds in a discernible but initially unforeseen manner.

“Bridge Breakage Fusion Cycle”

“Breakage Fusion Bridge Cycle”

Most of us would read [McClintock’s paper] and understand that it was going to be about chance events — events without predictable, programmatic, mechanistic responses. Not Perry Marshall!

A goal for the future would be to determine the extent of knowledge the cell has of itself, and how it utilizes this knowledge in a “thoughtful” manner when challenged.

Junk, gibberish with occasional bits of translated codes that convert to proteins with regulatory elements.

(From an older blog post by PZ, it was online in November but not present now)

Induction of such reprogrammings by insects, bacteria, fungi, and other organisms, which are not a required response of the plant genome at some stage in its life history, is quite astounding… It is becoming increasingly apparent that we know little of the potentials of a genome. Nevertheless, much evidence tells us that it must be vast.

I get confused and lost every time I read a bioinformatics paper — but these are scientists paid in big money and prestige to study genome function who don’t have a grasp on the evolutionary constraints on genome function, which seems to be a rather critical omission. (From another blog post)

The stimulus associated with placement of the insect egg into the leaf will initiate reprogramming of the plant’s genome, forcing it to make a unique structure adapted to the needs of the developing insect. The precise structural organization of a gall that gives it individuality must start with an initial stimulus, and each species provides its own specific stimulus. For each insect species the same distinctive reprogramming of the plant genome is seen to occur year-after-year.

PZ is telling you that transposons are genes that jump around randomly, for no apparent reason. What an impoverished view of science.

Transposons do not jump around randomly. McClintock is saying that mobile genetic elements move to change expression of genes in programmed ways in response to threats.

She is saying they follow predictable, precise, algorithmic patterns when known threats occur, and in far less predictable, but nonetheless orderly (ergodic), contextual ways when unpredictable threats occur.

PZ says, “Each daughter cell gets a random selection of the genes along that bridge. That’s the whole point. You’re trying to explain a random phenotype by looking for a randomization mechanism in the genome.”

Yes, the breaking of chromosomes is a random, damaging event. But the reconstruction of any chromosome is not! The cell is an editor given a text with broken fragments of sentences, which puts them back together in a semantically correct and functional way.

The Breakage-Fusion-Bridge cycle is a phase when the plant is struggling because the sentence is grammatically incorrect and thus useless to the reproductive system.

All you get by assuming the cell’s actions are random is: No reason to look deeper into anything. Randomness means “no pattern.” It is the end of the road, a declaration that there is no further structure or set of rules to discover and discern. A scientific brick wall.

Which is why Neo-Darwinism, with its outdated assumption of random mutations, is lazy man’s science.

PZ wants to tell you how dumb the genome is. McClintock dares to ask how smart it is.

Which scientist is doing their job? Which scientist is pushing an agenda?

When you assume the cell doing that for a reason, the scientist has a reason to move forward. Instead of declaring its behavior random, let’s find out why. Let’s uncover the system behind the pattern.

McClintock did that and won a Nobel Prize. PZ, you might get more grant money if you don’t assume the genome is “gibberish.” Nobody’s gonna pay you to rummage through gibberish.

Barbara would vehemently disagree with you, PZ. She doesn’t use words like “wise” and “thoughtful,” or refer to the cell’s knowledge of itself by accident. She knows exactly what she’s saying. It was her elevated view of life that afforded her many of the insights she is now renowned for.

Are these white blood cells dumb and purposeless? Or are they trying to eat these bacteria?

I submit to you, dear reader, that PZ is quote mining Barbara McClintock and twisting her discoveries to serve his agenda.

But don’t take my word for it. Read McClintock’s Nobel Prize paper and decide for yourself.

23 Responses

  1. Perry Marshall seems to be having a blog war with an unarmed opponent. It may be past time for all serious scientists to move forward by ignoring all neo-Darwinian teleophobes.
    They were “outed” more than 50 years ago, when Dobzhansky (1964) wrote: “It is a striking and profoundly meaningful fact that organisms are so constructed, so function, and so behave that they survive and perpetuate themselves in a certain range of environments frequently enough for their species not to become extinct for long periods of time. Furthermore, the ranges of the environments propitious for survival and reproduction are widely different for different forms of life. A biologist who chooses to ignore this widespread adaptedness overlooks a fundamental and very nearly universal characteristic of all that can be meaningfully studied on every level of biological integration, from the strictly molecular to the highest organismic the ecosystem level.” — p. 450
    http://www.jstor.org/stable/3881145?origin=JSTOR-pdf&seq=1#page_scan_tab_contents

    PZ Myers ignores everything known to serious scientists about the links from atoms to ecosystems. They must include nutrient energy-dependent RNA-mediated DNA repair and the physiology of reproduction. I hope Perry Marshall can find an intelligent blogger, or someone who wants to debate him at his level of competent accurate representations of biologically-based cause and effect.

  2. Jared Allen says:

    All you need to know about people like P.Z. Myers is that they’re motivated by their worldview (religion, really), not by an honest search for truth.

    People like Myers can’t accept the realities of living systems, because they know the implications of those realities: They crush everything atheists believe in.

    I think we both know nothing you write here will lead to Myers’ budging an inch; he’s taking his archaic science and irrational worldview to the grave. Still, you’re almost certainly pushing rational fence-sitters to the side of truth, so thank you for that.

  3. John says:

    Biology has memory. The longterm memory is the multigenerational natural selection shaped genome. The short term memory is methylization (epigenetics), again shaped by natural selection. Are we seeing computational capability of genetics? That should not be a surprise. Does that give us a reason to believe in biological teleology? No.

  4. This may seem to be too technical, but it is also worth watching if you think there is no reason to believe in biological teleology. For comparison to claims about random mutations and evolution, see what serious scientists know about DNA repair. https://www.facebook.com/AAMB.UK/videos/1103126899704279/ Then, thank Perry Marshall for helping you understand the complexity of DNA repair and cell type differentiation without all the technicalities.

  5. Dale Ferry says:

    You are being misled by the language and by failing to consider that four billion years is a very long time. Barbara McClintock was describing phenomena that were pretty poorly understood at the molecular level at the time. What you see now in terms of what goes on in cells are only the successful experiments that have occurred over four billion years of evolution. Yes DNA contains information but it isn’t information that anyone or thing ‘put’ there. It’s the infinite (or at least very large number) of typewriters set up to type letters at random. Every so often someone goes in and removes all the documents that don’t have an English word in them (or in the case of natural selection, cells and organisms which fail to reproduce are lost). The rest of the documents continue to grow. Four billion years later you decide that typewriters have developed intelligence because their documents contain so many English words.

    • Reading this, I have to wonder if you have a background in science or mathematics, in order for you to believe this is true. Especially when you bring up monkeys at typewriters.

      What is your mathematical background?

      • Dale Ferry says:

        I minored in math as an undergrad. Sorry you don’t like monkeys at typewriters. It’s hard to come up with a suitable analogy for a process that has no really appropriate analogy.

        • Do some math and show us whether the infinite monkey theorem actually can produce shakespeare in any reasonably finite universe.

          More specifically, please use statistics to show us exactly how much Shakespeare a trillion monkeys could produce in a trillion years.

          • Sir Paul Nurse has a better approach sans the monkeys.

            See: Life, logic and information http://www.nature.com/nature/journal/v454/n7203/full/454424a.html

            Excerpt: “A metaphor here would be the use of the Morse code and the telegraph to communicate messages. Pulses of information sent along the telegraph generate a code for letters and as a consequence sentences can be communicated. This converts the same signalling pathway from a simple on/off switch to a device that can transfer, for example, the works of Shakespeare. (p. 426) It is likely that dynamics has been exploited more generally in the evolution of biological systems for signalling purposes, allowing the communication of more complex information.”

            It is surprising to me to see people comment who will not bother to read your book to see what you have already addressed.

          • Eric says:

            I think the answer is 10^200000 keystrokes, squared if you include punctuation, which after rounding for a trillion monkeys, is about the same. But what if there’s a multiverse…How many of those are there supposed to be?

          • Dale Ferry says:

            I didn’t say Shakespeare, I said ‘some English words’, of which google tells me there are over a million. I think you would agree the latter doesn’t require infinite monkeys or time.

            • Why don’t you calculate this, based on an amount of English text that’s roughly comparable to information content of the genome of c. elegans. Run the math on that. What do you find?

              • Dale Ferry says:

                How do you propose to determine the informational content of the c. elegans genome? Its size is known but based on comparisions with other distantly related nematode species, there’s a lot of functional conservation even in stretches of DNA without sequence conservation. How much I don’t know because only very small regions of the genome have been studied in that way. Plus large swatches of the genome have been moved around in ways that would make English text completely incomprehensible. Undergrad math never taught me how to account for any of that.

                The analogy was never intended to be followed precisely. I was just trying to point out that the undirected nature of evolution is not apparent after 4 billion years because we can only see such a tiny glimpse of what happened along the way.

                • I’d be happy with the equivalent of the storage capacity of the genome, which might be something like 1MB.

                  Thus far in this conversation you’ve gone from making a mathematically absurd statement (which I was quite prepared nail you on) … to at this point not really saying anything at all.

                  Nobody with any level of mathematical education should be claiming that random mutation and natural selection alone (“monkeys with typewriters”) produce evolution. It’s an indefensible position, as it is demonstrably false.

                  Evolution is directed. Barbara McClintock showed this in the 1940s and 50s and explains in detail in her Nobel Prize speech.

                  • Dale Ferry says:

                    S. E. LURIA AND M. DELBRÜCK. Luria, S. E., and M. Delbrück, 1943. Mutations of bacteria from virus sensitivity to virus resistance. Genetics, 28: 491–511.

                    will explain the point I was trying to make better than I can.

                    • Dale,

                      The Delbruck Luria experiment doesn’t prove what people think it proves.

                      I’m going to get around to a question asked by Chris Wallis about this when I get time.

                      From the scientist who discovered transposons in bacteria:
                      http://www.huffingtonpost.com/james-a-shapiro/epigenetics-ii-cellular-m_b_1668820.html

                      quote:

                      The empirical evidence against experience-related genome change is remarkably thin. Textbooks present the famous 1943 Luria-Delbrück experiment as the definitive demonstration that mutations must occur prior to selection.

                      Salvador Luria and Max Delbrück, who received Nobel Prizes for their pioneering roles in molecular genetics, set out to test whether virus infection could induce mutations to resistance.

                      The analysis was statistical in nature. (Their paper even includes an elaborate mathematical appendix by Delbrück, a converted theoretical physicist.) The argument was as follows. If infection induced mutations to virus resistance with a certain low probability, then both different samples from one culture and samples from independent cultures should display similar numbers of colonies that would fit some form of normal (Gaussian) distribution.

                      They set up a large number of independent cultures of bacteria, divided them each into multiple samples, infected all samples with viruses that killed infected cells, and measured the frequency (proportion) of resistant mutant bacteria in each sample that could produce a colony in the presence of the lethal viruses.

                      What they found was that the replicas of single cultures did produce normal distributions of resistant colony numbers, as expected, but the colony numbers from one culture bore no statistical relationship to the other independent cultures. Some cultures produced very low numbers of colonies, while others displayed “jackpots” of high frequencies of resistant cells.

                      They correctly interpreted this deviation from a normal culture-to-culture distribution of mutant frequencies to provide evidence for the stochastic occurrence of rare mutations to virus resistance at different times in the growth of each culture prior to selection. Early mutations would multiply into many resistant progeny (high mutant frequency), while later-occurring mutations would produce smaller populations of resistant progeny (low mutant frequency).

                      Given the lethal nature of the selecting virus Luria and Delbrück used, there was in fact no other possible outcome. Infection was invariably lethal, and only preexisting resistant mutants could survive. Nonetheless, this experiment was cited for over six decades as proof that virus infection could not induce a genetic change to resistance.

                      One has to be careful with the word “proof” in science. I always said that conventional evolutionists were hanging a very heavy coat on a very thin peg in the way they cited Luria and Delbrück. The peg broke in the first decade of this century.

                      Bacterial genomicists noted some curious structures in the DNA sequences of many different bacterial species. They were called CRISPRs, for “clustered regularly interspaced short palindromic repeats.” The structures had groups of inverted repeat sequences (“palindromic repeats”) arranged near each other in a short region of the bacterial DNA.

                      Although their meaning was not known at first, the regularity of the CRISPRs made them literally pop out of the computer analysis. The functional significance of the CRISPRs became clearer when the non-repeat “spacer” segments separating the inverted repeats were analyzed. They contained short sequences from viruses, plasmids, and other types of invasive DNA. It looked like the CRISPR might serve as a kind of DNA memory bank for past infections of the bacterial cell.

                      Perhaps the CRISPR system provided not only memory but defense against infectious DNA. This idea was tested by infecting bacterial cells with viruses that are not invariably lethal, and it was found to be correct. The surviving bacteria had new repeats and spacers in their CRISPRs, and the spacers contained DNA sequence fragments from the infecting viruses.

                      The “impossible” had happened. By a still-unknown mechanism, the bacterial cell managed to insert a short sequence from the infecting virus in its genome’s CRISPR region and use that newly acquired information to block the infection. There is now evidence that the CRISPR defense works by encoding a small interfering RNA molecule (siRNA) and using that siRNA to guide cleavage of the invading DNA.

                      This remarkable CRISPR genome immunity system is an example of the general, recently discovered process known as “RNA interference,” or RNAi. RNAi regulates genome expression in eukaryotic cells by targeting the destruction of transcripts from coding sequence, but RNAi also targets the formation of silenced chromatin and so blocks transcription in the first place.

  6. Carol Sperling says:

    Perry,
    Does your NDA require consent of both parties before the substance of a submitted prize attempt can be publicly disclosed?

  7. See also: How the cell’s power station survives attacks http://medicalxpress.com/news/2016-01-cell-power-station-survives.html

    “Evolution 2.0” helps others to understand how RNA-mediated DNA repair protects organized genomes from stress-linked damage.

    But first, teleophobes must accept the fact that all serious scientists know that DNA repair is required.

    See, for example: Study connects mitochondria to psychological stress response and species resilience http://medicalxpress.com/news/2015-11-mitochondria-psychological-stress-response-species.html#nRlv

  8. Dale Ferry says:

    “The “impossible” had happened. By a still-unknown mechanism, the bacterial cell managed to insert a short sequence from the infecting virus in its genome’s CRISPR region and use that newly acquired information to block the infection. ”

    Except that makes it sound as if exposing a single bacterial cell containing CRISPR/cas sequences to a virus and will result in a viral resistant cell. It doesn’t. Exposing 10 or a 100 or a 1000 or even a million cells doesn’t result in a viral resistant cell most of the time. Exposing a billion cells will do it because it’s the result of chemistry and an undirected process. The few successes will grow and the rest of the billion cells will die.

    • Run the math, Dale, and you’ll figure out one in a billion is too frequent a success rate to ascribe to chance. (Even if you’re right and I’m not sure you are.)

      By the way, you lied about your math background. You have no math expertise as far as I can tell.

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